Does mucilage worsen Crohn's?

Mucilage from Wikipedia

Aloe vera
Basella alba (Malabar spinach)
Cactus
Chondrus crispus (Irish moss) AKA carrageenen (see my post entitled  "Does carrageenan worsen Crohn's?"
Dioscorea opposita (nagaimo, Chinese yam)
Drosera (sundews)
Drosophyllum lusitanicum
Fenugreek
Flax seeds
Kelp
Liquorice root
Marshmallow
Mallow
Mullein
Okra
Parthenium
Pinguicula (butterwort)
Psyllium seed husks
Salvia hispanica (chia) seed
Ulmus rubra bark (slippery elm)

Exopolysaccharide from Wikipedia
"Exopolysaccharides generally consist of monosaccharides and some non-carbohydrate substituents (such as acetate, pyruvate, succinate, and phosphate)"

Does the soothing action of demulcents outweigh the inflammation stimulated by polysaccharides?

(At our house, the answer is NO!)

Does smoking improve Crohn's?

"'Doctors don't always know best:' Student claims he cured debilitating bowel disease by taking up smoking" in Daily Mail
"A medical student claims to have cured himself of a debilitating disease by taking up smoking.
Formerly a non-smoker, Stephen Pendry, 23, struggled with crippling pain, tiredness, shortness of breath and dehydration since he was diagnosed with bowel disease ulcerative colitis four years ago.
He had to rush to the toilet up to 15 times a day but is now completely symptom-free, thanks to a new four-a-day cigarette habit.
The incredible turnaround is due to a side-effect of nicotine, hardly known outside medical circles, which cancels out damage caused by the disease."

"Anti-inflammatory effects of nicotine in obesity and ulcerative colitis" in Journal of Translational Medicine (2011)
"Much work remains in terms of understanding the anti-inflammatory effects of nicotine in obesity-related inflammation and ulcerative colitis. However, it is now known that the α7nAChR plays a major role in the anti-inflammatory effects of nicotine and nicotine attenuates inflammation in both obesity and ulcerative colitis. What these findings suggest is the potential use of selective α7nAChR agonists as a new class of anti-inflammatory drugs. Despite tremendous efforts, obesity and obesity-related disorders remain at epidemic proportions and the etiology of ulcerative colitis remains unclear. Since the inflammatory response is an integral process in both obesity and ulcerative colitis, controlling the inflammatory response could ameliorate tissue damage. The effectiveness of α7nAChR agonists as a drug target will ultimately depend upon a clear understanding of the collective biological consequences of peripheral nAChR expression on inflammation. In addition, it should also be considered that the development of nicotine as a therapeutic intervention has its limitations due to toxicity related side effects and pharmacological non-specificity."

"Does nicotine influence cytokine profile and subsequent cell cycling/apoptotic responses in inflammatory bowel disease?" in Inflammatory Bowel Diseases (2008)
"Dysregulated cytokine profiles in UC and CD are associated with specific alterations in cell cycle responses; these effects may be modified by nicotine, and potentially by anticytokine therapies."

With Crohn's, is it better to be GMO-free?

GMO foods from Greenpeace Canada
"GE food has been in grocery stores since 1996, but no long-term tests have been done on the impacts on human health. Potential health risks include the development of antibiotic resistance, allergic reactions, nutritional changes and the creation of toxins. GE crops also threaten plant diversity, essential for food security."

Do FODMAPs cause Crohn's?

Personal view: food for thought – western lifestyle and susceptibility to Crohn's disease. The FODMAP hypothesis, Gibson in Alimentary Pharmacology and Therapeutics (2005)
"A new hypothesis is proposed, by which excessive delivery of highly fermentable but poorly absorbed short-chain carbohydrates and polyols (designated FODMAPs – Fermentable Oligo-, Di- and Mono-saccharides And Polyols) to the distal small intestinal and colonic lumen is a dietary factor underlying susceptibility to Crohn's disease. The subsequent rapid fermentation of FODMAPs in the distal small and proximal large intestine induces conditions in the bowel that lead to increased intestinal permeability, a predisposing factor to the development of Crohn's disease. Evidence supporting this hypothesis includes the increasing intake of FODMAPs in western societies, the association of increased intake of sugars in the development of Crohn's disease, and the previously documented effects of the ingestion of excessive FODMAPs on the bowel. This hypothesis provides potential for the design of preventive strategies and raises concern about current enthusiasm for putative health-promoting effects of FODMAPs."

"FODMAPs might be considered the ‘fast food’ for bacteria."

"Review article: fructose malabsorption and the bigger picture" in Alimentary Pharmacology & Therapeutics (2007)
" A preliminary report has indicated that application of the FODMAP approach and dietary intervention in patients with Crohn's disease has had symptomatic benefit in a high proportion.91 Likewise, reducing FODMAP intake may lead to improved pouch function in patients with an ileo-anal pouch anastomosis. ... FODMAPs have been recently hypothesized to play a role in the pathogenesis of Crohn's disease and have been speculatively linked to the increased prevalence of Crohn's disease in Western countries.21 While evidence to support such a contention is limited, it does warrant serious consideration because such factor is amenable to preventive measures. ... The concept of fructose malabsorption has been generally poorly understood in the gastroenterological community, perhaps to a large extent due to its being considered an illness or abnormality, and due to the lack of awareness of dietary fructans in the genesis of symptoms."

Does monosodium glutinate worsen Crohn's symptoms?